Inflammatory bowel disease (IBD) is a serious disease of humans, the pathogenesis of which has not been fully elucidated. Rhesus macaques diagnosed with a spontaneously occurring chronic colits were evalutated as a possible nonhuman primate model of human IBD. We have previously shown that macaques with chronic colitis show increased levels of nitric oxide (NO) metabolic intermediates in plasma and urine, and have increased inducible nitric oxide synthase (iNOS) gene expression in situ in the colon. Current studies are an extension of experiments to investigate the role of endogenous NO in the pathogenesis of colonic inflammation in a primate model system, and evaluate the efficacy of a iNOS inhibitor, aminoguanidine, as a treatment modality. Animals were enrolled in the study as they were diagnosed. Baseline pre-treatment colonic biopsy samples, and plasma/serum samples were obtained. Animals were randomly assigned to treatment or control groups, receiving 10 consecutive days of treatment with aminoguanidine or sham treatment with saline, respectively. Plasma and urine samples were collected on days 5 and 10 from both treated and controls. All animals were euthanatized and colonic tissues collected for histopathologic examination. Slight to moderate improvement, based on decreased iNOS gene expression from baseline in colonic tissues, was observed in animals treated with aminoquanidine compared to controls. While the results were not dramatic, the utility of this model system for evaluation of longer treatment regimens, or other more potent iNOS inhibiting compounds has been demonstrated. *KEY*Nitric oxide, Colitis, Macaques, Inflammatory bowel disease, Therapy